'Dessert Stomach' Is Real And It Lives in Your Brain

Couldn't eat another bite, but definitely have room for a slice or two of that oh-so-moist triple chocolate ganache cake? This is the paradox of the "dessert stomach."

A new study from the Max Planck Institute for Metabolism Research in Cologne, Germany has confirmed that the dessert stomach phenomenon is real—and it lives in your brain.

"From an evolutionary perspective, this makes sense: sugar is rare in nature, but provides quick energy," explained paper author and neurobiologist Henning Fenselau in a statement.

"The brain is programmed to control the intake of sugar whenever it is available."

In their study, Fenselau and colleagues started out exploring how mice reacted to sugar even if they were completely satiated. Like us, they also seemed to always have room for dessert.

Monitoring the rodents' brains, the team found that a group of appetite and regulating nerve cells called the pro-opiomelanocortin (PMOC) neurons lit up as soon as the mice were given sugar, and enabled their appetite.

According to the researchers, when the mice were full but also ate sugar, the PMOC neurons not only release signaling molecules to tell the body it was satiated, but also a bodily opiate, ß-endorphin.

ß-endorphin acts on certain other nerve cells with opiate receptors to trigger a feeling of reward—and it is this that encouraged the mice to keep eating although they were already full.

Notably, this opiate pathway was not activated in the rodents' brains when they were given additional regular or fatty food, rather than sugar; and when the pathway was blocked, full mice seemed to lose their metaphorical dessert stomachs and did not eat extra sugar.

Blocking ß-endorphin release had no effect on hungry mice who had not eaten.

In a follow-up experiment, this time on humans, the researchers performed brain scans on volunteers who were given a sugar solution through a tube.

The scans revealed that the same part of the human brain reacts to sugar as in the mice—with the "dessert stomach" region in both species featuring satiety neurons in close proximity to opiate receptors.

The findings, the team said, could help in the treatment of obesity in the future.

"There are already drugs that block opiate receptors in the brain, but the weight loss is less than with appetite-suppressant injections," Fenselau noted.

"We believe that a combination with them or with other therapies could be very useful. However, we need to investigate this further."

In fact, Fenselau adds, this is just one area of future investigation they are planning.

"There still a lot of open questions we are planning to address," he told Newsweek.

"For example, what happens in obesity? Is this opioid pathway contributing to its development? And, how does obesity affect its function?"

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Update 02/14/25, 12:43 p.m. ET: This article was updated with additional comments from Henning Fenselau.

Reference

Minère, M., Wilhelms, H., Kuzmanovic, B., Lundh, S., Fusca, D., Claßen, A., Shtiglitz, S., Prilutski, Y., Talpir, I., Tian, L., Kieffer, B., Davis, J., Kloppenburg, P., Tittgemeyer, M., Livneh, Y., & Fenselau, H. (2025). Thalamic opioids from POMC satiety neurons switch on sugar appetite. Science, 387(6735). https://doi.org/10.1126/science.adp1510